| Hepatitis B Virus (HBV) infection is associated with a variety of clinical manifestations ranging from asymptomatic carrier, fulminant hepatitis, chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. Persisitent HBV infection has been considered as a multifactorial and polygenic disorder with viral, environmental and genetic components. HBV genomic variability and a number of conventional risk factors, including age, gender, concurrent infection with the hepatitis C virus (HCV), hepatitis D virus (HDV) and human immune deficiency virus (HIV), are clearly the important factors contributing to the incidence of persistent HBV infection. However, segregation analysis and twin studies strongly support the role of host genetic components in determining the chronicity of HBV infection. A known and unknown number of identified or unidentified genes are likely to modify the susceptibility to persistent HBV infection. Single nucleotide polymorphism (SNP) is a powerful tool for identifying genetic susceptibilities to common complex diseases in recent years.This study aimed at characterizing gene polymorphisms in position 1176G/C in intron4 of HMGB1894G/T in exon7 of eNOS, 18109T/C in exon20 of HMGCR, -1285T/A in promoter and 111T/C in exon1 of FGL2 among patients with hepatitis B virus (HBV) infection. The results showed that:1. The observed gene polymorphisms existed in the patients were in Hardy-Weinberg equilibrium. The allele frequency except in FGL2 111T/C position (the allele frequency is 0) was more than 5%, so we could detect the SNP in a large scale except in position 111T/C of FGL2.2. The results reflected there was statistically significant evidence of association between HMGB1 1176G/C SNP and HBV: the fraction calculated by relative risk indicated that HMGB1 1176G/G genotype can be attributed to be more susceptible to CHB, LC, SHB than 1176C/C and 1176G/C genotypes. In other words,patients with 1176G/G genotype of...
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